Jung, Seung Wook;Kim, Yeon Jae;Kim, Gun Hyun;Kim, Min Seon;Son, Hyuk Soo;Kim, Jun Chul;Ryu, Hyon Uk;Lee, Soo Ok;Jung, Chi Young;Lee, Byung Ki
Tuberculosis and Respiratory Diseases
/
v.59
no.4
/
pp.368-373
/
2005
Background : Bronchial anthracofibrosis usually manifest as a form of obstructive airway disease, and can be accompanied by parenchymal diseases such as pneumonia, and pulmonary tuberculosis. This study investigated the ventilatory dynamics according to the severity of bronchial stenosis in patients with bronchial anthracofibrosis. Method : One hundred and thirteen patients with bronchial anthracofibrosis that was confirmed by bronchoscopy and who had undergone a pulmonary function test were enrolled in this study group. The correlation coefficients between the pulmonary functional parameters and the number of lobes with bronchial stenosis were investigated. Results : The incidence of ventilatory dysfunction was 56(49.6%) for obstructive, 8(7.1%) for restrictive, 2(1.8%) for mixed, and 47(41.6%) for a normal pattern. The $FEV_1/FVC$, $FEF_{25{\sim}75%}$, $FEF_{25%}$, $FEF_{50%}$, $FEF_{75%}$, and PEF showed a significant negative correlation (p<0.05) and the Raw had a significant positive correlation with the number of lobes with bronchial stenosis(p<0.001). Conclusion : These findings suggest that the most common abnormality of the ventilatory function in bronchial anthracofibrosis is an obstructive pattern with a small airway dysfunction according to the severity of bronchial stenosis.
Background : Obstructive sleep apnea syndrome (OSAS) affects systemic blood pressure and cardiac function. The development of cardiovascular dysfunction including the changes of systemic blood pressure and cardiac rhythm, suggests that recurrent hypoxia and arousals from sleep may increase a sympathetic nervous system activity. Continuous positive airway pressure (CPAP) therapy has been found to be an effective treatment of OSAS. However, only a few studies have investigated the cardiovascular and sympathetic effects of CPAP therapy. We evaluated influences of nasal CPAP therapy on the cardiovascular system and the sympathetic activity in patients with OSAS. Methods : Thirteen patients with OSAS underwent CPAP therapy and were monitored using polysomnography, blood pressure, heart rate, presence of arrhythmia and the concentration of plasma catecholamines, before and with CPAP therapy. Results: The apnea-hypopnea index (AHI) was significant1y decreased (p<0.01) and the lowest arterial oxygen saturation level was elevated significantly after applying CPAP (p<0.01). Systolic blood pressure tended to decrease after CPAP but without statistical significance. Heart rates during sleep were not significantly different after CPAP. However, the frequency and number of types of arrhythmia decreased and sinus bradytachyarrhythmia disappeared after CPAP. Although there was no significant difference in the level of plasma epinephrine concentration, plasma norepinephrine concentration significantly decreased after CPAP (p<0.05). Conclusion : CPAP therapy decreased the apnea-hypopnea index, hypoxic episodes and plasma norepinephrine concentration. In addition, it decreased the incidence of arrhythmia and tended to decrease the systemic blood pressure. These results indicate that CPAP may play an important role in the prevention of cardiovascular complications in patients with OSAS.
Background: The existing data indicate that obstructive sleep apnea syndrome contributes to the development of cardiovascular dysfunction such as systemic hypertension and cardiac arrhythmias, and the cardiovascular dysfunction has a major effect on high long-term mortality rate in obstructive sleep apnea syndrome patients. To a large extent the various studies have helped to clarify the pathophysiology of obstructive sleep apnea, but many basic questions still remain unanswered. Methods: In this study, the influence of obstructive sleep apnea on systemic blood pressure, cardiac rhythm and urinary catecholamines concentration was evaluated. Over-night polysomnography, 24-hour ambulatory blood pressure and ECG monitoring, and measurement of urinary catecholamines, norepinephrine (UNE) and epinephrine (UEP), during waking and sleep were undertaken in obstructive sleep apnea syndrome patients group (OSAS, n=29) and control group (Control, n=25). Results: 1) In OSAS and Control, UNE and UEP concentrations during sleep were significantly lower than during waking (P<0.01). In UNE concentrations during sleep, OSAS showed higher levels compare to Control (P<0.05). 2) In OSAS, there was a increasing tendency of the number of non-dipper of nocturnal blood pressure compare to Control (P=0.089). 3) In both group (n=54), mean systolic blood pressure during waking and sleep showed significant correlation with polysomnographic data including apnea index (AI), apnea-hypopnea index (AHI), arterial oxygen saturation nadir ($SaO_2$ nadir) and degree of oxygen desaturation (DOD). And UNE concentrations during sleep were correlated with AI, AHI, $SaO_2$ nadir, DOD and mean diastolic blood pressure during sleep. 4) In OSAS with AI>20 (n==14), there was a significant difference of heart rates before, during and after apneic events (P<0.01), and these changes of heart rates were correlated with the duration of apnea (P<0.01). The difference of heart rates between apneic and postapneic period (${\Delta}HR$) was significantly correlated with the difference of arterial oxygen saturation between before and after apneic event (${\Delta}SaO_2$) (r=0.223, P<0.001). 5) There was no significant difference in the incidence of cardiac arrhythmias between OSAS and Control In Control, the incidence of ventricular ectopy during sleep was significantly lower than during waking. But in OSAS, there was no difference between during waking and sleep. Conclusion : These results suggested that recurrent hypoxia and arousals from sleep in patients with obstructive sleep apnea syndrome may increase sympathetic nervous system activity, and recurrent hypoxia and increased sympathetic nervous system activity could contribute to the development of cardiovascular dysfunction including the changes of systemic blood pressure and cardiac function.
Background : The dominant innervation of airway smooth muscle is parasympathetic fibers which are carried in the vagus nerve. Activation of these cholinergic nerves releases acetylcholine which binds to $M_3$ muscarinic receptors on the smooth muscle causing bronchocontraction. Acetylcholine also feeds back onto neuronal $M_2$ muscarinic receptors located on the postganglionic cholinergic nerves. Stimulation of these receptors further inhibits acetylcholine release, so these $M_2$, muscarinic receptors act as autoreceptors. Loss of function of these $M_2$ receptors, as it occurs in animal models of hyperresponsiveness, leads to an increase in vagally mediated hyperresponsiveness. However, there are limited data pertaining to whether there are dysfunctions of these receptors in patients with asthma. The aim of this study is to determine whether there are dysfunction of $M_2$ muscarinic receptors in asthmatic patients and difference of function of these receptors according to severity of asthma. Method : We studied twenty-seven patients with asthma who were registered at Pulmonology Division of Korea University Hospital. They all met asthma criteria of ATS. Of these patients, eleven patients were categorized as having mild asthma, eight patients moderate asthma and eight patients severe asthma according to severity by NAEPP Expert Panel Report 2(1997). All subjects were free of recent upper respiratory tract infection within 2 weeks and showed positive methacholine challenge test ($PC_{20}$<16mg/ml). Methacholine provocation tests were performed twice on separate days allowing for an interval of one week. In the second test, pretreatment with the $M_2$ muscarinic receptor agonist pilocarpine($180{\mu}g$) through inhalation was performed be fore the routine procedures. Results : Eleven subjects with mild asthma and eight subjects with moderate asthma showed significant increase of $PC_{20}$ from 5.30$\pm$5.23mg/ml(mean$\pm$SD) to 20.82$\pm$22.56mg/ml(p=0.004) and from 2.79$\pm$1.51mg/ml to 4.67$\pm$3.53mg/ml(p=0.012) after pilocarpine inhalation, respectively. However, in the eight subjects with severe asthma significant increase of $PC_{20}$ from l.76$\pm$1.50mg/ml to 3.18$\pm$4.03mg/ml(p=0.161) after pilocarpine inhalation was not found. Conclusion : In subjects with mild and moderate asthma, function of $M_2$ muscarinic receptors was normal, but there was a dysfunction of these receptors in subjects with severe asthma. ηlese results suggest that function of $M_2$ muscarinic receptors is different according to severity of asthma.
Background: Endothelin(ET) is the most potent vasoconstrictor and bronchoconstrictor. The plasma ET-1 level is elevated in patients with acute pulmonary thromboembolism(APTE). This finding suggest that ET-1 may be an important mediator in the cardiopulmonary derangement of APTE. But whether ET-1 is a pathogenic mediator or a simple marker of APTE is not known. The role of ET-1 in the pathogenesis of cardiopulmonary dysfunction in APTE(delete) was investigated through an evaluation of the effects of $ET_A$-receptor antagonist on APTE. The increase in local levels of preproET-1 mRNA and ET-1 peptide in the embolized lung was also demonstrated. Methods: In a canine autologous blood clot pulmonary embolism model, $ET_A$-receptor antagonist(10 mg/kg intravenously, n=6) was administered one hour after the onset of the embolism. Hemodynamic measurements, blood gas tensions and plasma levels of ET-1 immunoreactivity in this treatment group were compared with those in the control group(n=5). After the experiment., preproET-1 mRNA expression(using Northern blot analysis) and the distribution of ET-1(by immunohistochemical analysis) in the lung tissues were examined. Results: The increases in pulmonary arterial pressure and pulmonary vascular resistance of the treatment group were less than those of the control group. Decrease in cardiac output was also less in the treatment group. Complications such as systemic arterial hypotension and hypoxemia did not occur with the administration of $ET_A$-receptor antagonist The plasma level of ET-1 like(ED: what does 'like' mean?) immunoreactivity was increased after embolization in both groups but was significantly higher in the treatment group. The preproET-1 mRNA and ET-1 peptide expressions were increased in the embolized lung. Conclusion: ET-1 synthesis increases with embolization in the lung and may plays play an important role in the pathophysiology of cardiopulmonary derangement of APTE. Furthermore, $ET_A$-receptor antagonist attenuates cardiopulmonary alterations seen in APTE, suggesting a potential benefit of this therapy.
Background : Chronic cough, defined as a cough persisting for three weeks or longer, is a common symptom for which outpatient care is sought. The most common etiologies of chronic cough are postnasal drip, asthma, and gastroesophageal reflux. Methacholine challenge is a useful diagnostic study in the evaulation of chronic cough, particularly useful in chronic cough patients with asthmatic symptom. Patients with chronic cough may have dysfunction of bronchial and extrathoracic airways. To evaluate if dysfunction of the bronchial and extrathoracic airways causes chronic cough, we assessed bronchial (BHR) and extrathoracic airway (EAHR) responsiveness to inhaled methacholine in patients with chronic cough. Method : 111 patients with chronic cough were enrolled in our study. Enrolled patients had no recorded diagnosis of asthma, bronchopulmonary disease, hypertension, heart disease or systemic disease and no current treatment with bronchodilator or corticosteroid. Enrolled patients consisted of 46 patients with cough alone, 24 patients with wheeze, 22 patients with dyspnea, 19 patients with wheeze and dyspnea. The inhaled methacholine concentrations causing a 20% fall in forced expiratory volume in 1s($PC_{20}FEV_1$) and 25% fall in maximal mid-inspiratory flow ($PC_{25}MIF_{50}$) were used as bronchial and extra thoracic hyperresponsiveness. Results : There were four response patterns to methacholine challenge study : BHR in 27 patients, EAHR in 16 patients, combined BHR and EAHR in 8 patients, and no hyperresponsiveness in 60 patients. In patients with cough alone, there were BHR in 3 patients, EAHR in 9 patients, and combined BHR and EAHR in 2 patients. In patients with wheeze and/or dyspnea, there were BHR in 24 patients, EAHR in 7 patients, and BHR and EAHR in 6 patients. Compared with patients with wheeze and/or dyspnea, patients with cough alone had more common EAHR than BHR. In patients with wheeze and/or dyspnea, BHR was more common than EAHR. Conclusion : These results show that among patients with hyperresponsiveness to methacholine, those with dyspnea and/or wheezing had mainly bronchial hyperresponsiveness, whereas those with chronic cough alone had mainly extrathoracic airway hyperresponsiveness.
Kim, Kang Ho;Park, Hong-Hoon;Kim, Esther;Cheon, Seok-Cheol;Lee, Ji Hyun;Lee, Stephen YongGu;Lee, Ji-Hyun;Kim, In Jai;Cha, Dong-Hoon;Kim, Sehyun;Choi, Jeongeun;Hong, Sang-Bum
Tuberculosis and Respiratory Diseases
/
v.54
no.3
/
pp.311-319
/
2003
Background : Previous studies have suggested that a B-type natriuretic peptide(BNP) test can provide important information on diagnosis, as well as predicting the severity and prognosis of heart failure. Myocardial dysfunction is often observed in critically ill noncardiac patients admitted to the Intensive Care Unit, and the prognosis of the myocardial dysfunction needs to be determined. This study evaluated the predictability of BNP on the prognosis of critically ill noncardiac patients. Methods : 32 ICU patients, who were hospitalized from June to October 2002 and in whom the BNP test was evaluated, were enrolled in this study. The exclusion criteria included the conditions that could increase the BNP levels irrespective of the severity, such as congestive heart failure, atrial fibrillation, ischemic heart disease, and renal insufficiencies. A triage B-Type Natriuretic Peptide test with a RIA-kit was used for the fluorescence immunoassay of BNP test. In addition, the acute physiology and the chronic health evaluation (APACHE) II score and mortality were recorded. Results : There were 16 males and 16 females enrolled in this study. The mean age was 59 years old. The mean BNP levels between the ICU patients and control were significantly different ($186.7{\pm}274.1$ pg/mL vs. $19.9{\pm}21.3$ pg/mL, p=0.033). Among the ICU patients, there were 14(44----) patients with BNP levels above 100 pg/mL. The APACHE II score was $16.5{\pm}7.6$. In addition, there were 11 mortalities reported. The correlation between the BNP and APACHE II score, between the BNP and mortality were significant (r=0.443, p=0.011 & r=0.530, p=0.002). The mean BNP levels between the dead and alive groups were significantly different ($384.1{\pm}401.7$ pg/mL vs. $83.2{\pm}55.8$ pg/mL p=0.033). However, the $PaO_2/FiO_2$ did not significantly correlate with the BNP level. Conclusion : This study evaluated the BNP level was elevated in critically ill, noncardiac patients. The BNP level could be a useful, noninvasive tool for predicting the prognosis of the critically ill, noncardiac patients.
After cardiac surgery, it has been recognized that various complications were associated with injured humoral and cellular immunity by cardiopulmonary bypass(CPB). Especially, in postoperative pulmonary dysfunction, transpulmonary leukostasis followed complement activation and inflammatory responses are major pathogen. Some studies have showed that pretreated-corticosteroids before CPB protected postoperative pulmonary dysfunction. Corticosteroids may inhibit complement and leukocyte activation. On based previous studies, present investigator determined changes of leukocyte counts and transpulmonary leukostasis during cardiac surgery and postoperative periods. For the evaluation of postoperative pulmonary function and edema, $PaO_2$ and chest X-ray were compared between pre-CPB and post-CPB. Fever and other parameters were also observed postoperatively. The aim of this study was to define for the prophylactic effects of corticosteroid(Solu-Medrol: 30mg/kg) on all the researched parameters. This study was prospectively designed with randomized-blind fashion for 50 patients undergoing cardiac surgery. According to the purpose of study, all patients were divided into placebo and steroid group. : Placebo group was 25 patients received normal saline(not corticosteroid), and steroid group was 25patients received corticosteroid(Solu-Medrol: 30mg/kg) before initiation of CPB. The results of study were summarized as follows. 1. Total peripheral leukocyte counts decreased significantly at 5 minutes of CPB in all patients(P<0.01), and began to increase progressively at later periods of CPB with neutrophilia. The significant rise remained at postoperative 7th day(P<0.05). 2. During partial CPB, transpulmonary leukostasis occurred in placebo group(P<0.001), whereas it was prevented in steroid group. 3. In both groups, peripheral lymphocyte counts were stable during CPB, but began to reduce at time of intensive care unit(ICU) and the lymphocytopenia remained until postoperative 3rd day. The lymphocyte counts recovered on postoperative 7th day. 4. In both groups, peripheral counts of monocyte were relatively stable in the early peroid of CPB, and increased gradually in the later periods of CPB. This significant monocytosis remained throughout postoperlative periods(P<0.05). 5. The mean value of postoperative $paO)_2$ was lower than that of pre-CPB in placebo group(P=0.01) but didn't significant in steroid group(P=0.90). In the incidence of pulmonary edema signs and fever, placebo group was higher than steroid group(P=0.001, p=0.01, respectively). However mechanical respiratory supporting and care periods at intensive care unit were not significant difference between two groups(P>.0.05).With the above results, the investigator concluded that leukocyte activation and pulmonary sequestration were caused by cardiac surgery with CPB and demonstrated that high dose corticosteroid will provide prophylactic effect for pulmonary leukostasis and higher neutrophilia. These effects may ameliorate postoperative pulmonary dysfunction and contribute to postoperative less morbidity. However, further study should be performed because postoperative lymphocytopenia continued for 3 days in both groups, which may suspected damage or suppression of cell-mediated immunity with used corticosteroid.
Kim, Joon Young;Lee, Eun Seob;Bang, Ji Seok;Oh, Yeon Joung;Lee, Yong Ju;Sung, Tae-Jung;Lee, Kon-Hee;Lee, Jung Won
Childhood Kidney Diseases
/
v.18
no.2
/
pp.71-76
/
2014
Purpose: Attention deficit hyperactivity disorder (ADHD) has been associated with impairments in frontal inhibitory function and the catecholaminergic system. ADHD is diagnosed in 3-5% of children. Children with ADHD seem develop various forms of urinary problems such as nocturnal enuresis, dysfunctional voiding, and diurnal incontinence. However, no data exist to confirm the presence of these problems in Korean children with ADHD. We investigated the clinical findings of voiding dysfunction in children with ADHD. Methods: Between October 2009 and March 2011, a total of 63 children (33 with ADHD, 30 with an upper respiratory infection, as a control group) were enrolled. ADHD was diagnosed using the diagnostic and statistical manual of mental disorders (DSM)-IV criteria. A comprehensive survey of voiding and defecation was administered. Results: The patient group included 28 boys and 5 girls; the control group comprised 20 boys and 10 girls. The mean age was $9.09{\pm}2.8$ years in the ADHD group and $8.58{\pm}3.1$ years in the control group. Children with ADHD had a statistically significantly higher incidence of urgency (P =0.017), urge incontinence (P =0.033), and constipation (P =0.045). There was no significant difference in the incidence of straining, intermittency, holding maneuvers, or nocturnal enuresis. Conclusion: Children with ADHD in Korea have significantly higher rates of urgency, urge incontinence, and constipation than those without ADHD.
Backgroud. To determine the influence of age at operation upon surgical outcome in patients with isolated secundum atrial septal defect, retrospective clinical analysis was done. Material and method. From June, 1976 to December, 1991, 146 patients, 63 male and 83 female patients ranging in age from 13 months to 56 years, were operated on for isolated secundum atrial septal defect. The patients were divided into 3 groups according to their age at operation: Group I [<20 years old], 91 patients[62.3%]; Group II [21 to 40 years old], 44 patients[30.1%]; GroupIII[>41 years old], 11 patients[7.6%]. Significant differences in clinical features, hemodynamic function, early and late results between age groups were speculated. Results. One hundred thirty-one patients[89.6%] were symptomatic at the time of operation, the most common symptoms being dyspnea on exertion, recurrent respiratory infection, palpitation and chest pain. Patients in NYHA class III or IV were 3.3% in group I, 25% in groupIII, and 54.5% in group Ill. Hemodynamic data was available for 138 patients [94.5%]. Significant pulmonary hypertension [MPA systolic pressure $^3$ 40mmHg] was noted in 22 patients [15.9%]. Patients with pulmonary vascular disease [Rp/Rs>1.25] were 2% in group I, 7.3% in group Il, and 9.1% in groupIII. But there were no significant differences between the age groups in the size of the shunt or the ratio of pulmonary to systemic flow. Atrial septal defects were closed with direct suture in 144 patients and patch repair was performed in 2 patients with high defect. Atrial arrhythmia [8.2%] was the most common postoperative complication. The mean [LSD] duration of follow-up in all patients was 16$\pm$22 months [range, 1~96 months]. Functional result was excellent regardless of the age groups. During follow-up period, late cardiovascular events were arrhythmia [7 cases], reoperation for recurrent ASD [2 cases], and premature late death due to bacterial endocarditis [1 case]. Incidence of preoperative and late atrial fibrillation was significantly higher in older age group. Conclusion. Age at operation is one of the most important predictor of early and late surgical outcome with its impact on the following factors : 1] hemodynamic alterations and ventricular dysfunction due to longstanding volume and pressure overload, 2] pulmonary vascular disease, and 3] atrial arrhythmia including atrial fibrillation as a result of atrial dilatation. Therefore, among patients with surgically repaired atrial septal defects, those operated on over the age of 20 require careful supervision on the long-term basis.
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